Environmental Triggers of Asthma

Upon completion of this section, you will be able to

• Identify five indoor triggers of an acute asthma episode,
• Identify five outdoor triggers of an acute asthma episode, and
• Describe the impact of occupational exposures on adult asthma prevalence.

Exposure to many environmental factors can trigger and exacerbate asthma. The American Academy of Pediatrics has published a book about childhood environmental health problems, which states: “Avoiding environmental allergens and irritants is one of the primary goals of good asthma management” [AAPCEH 2003].

Medical and nursing education programs often do not fully incorporate environmental questions and an exposure history into asthma management. A recent study reported that, although over half of practicing pediatricians surveyed had seen a patient with health issues related to environmental exposures, fewer than 1/5th were trained in taking an environmental history [Kilpatrick et al. 2002].

This Case Study focuses on

• Allergens such as
  • Pollen,
  • Mold,
  • Animal dander,
  • Insect parts, and
  • Some chemicals
• Irritants such as
  • Smoke,
  • Dust,
  • Gas or Diesel fumes, and
  • Chlorine

which can trigger or exacerbate an asthma attack in individuals with increased airway hyper responsiveness.

How an environmental pollutant may affect asthma severity [IOM 2000].

• The pollutant might act as an inciter or trigger, leading to an asthma attack in an individual with hyper-responsive airways.
• The pollutant can exacerbate pre-existing airway inflammation, leading to increased airway hyper-responsiveness, which may persist after exposure ends.
• The pollutant might augment or modify immune responses to inhaled antigens or intensify the effect of other pollutants in the respiratory tract.

Several studies support the importance of allergies and allergens in triggering and exacerbating asthma. Key findings include

• Sensitization to indoor allergens and the spores of outdoor molds is a risk factor for the development of asthma in children and adults.
• In children and adults, sensitive to indoor allergens, the severity of asthma symptoms may vary with the level of exposure.
• Reduction of exposure to house-dust mites has improved Pulmonary Function Tests (PFTs) results and reduction in airway inflammation and hyper-responsiveness in sensitive children and adults [Nelson 2000; Frew 2003a; Simpson and Custovic 2004].

Taken together, these studies make a strong argument for the importance of allergen and irritant exposure as aggravating factors in asthma in both children and adults. The findings reinforce the importance of the identification and treatment of these exposures.

In industrialized countries, adults and children often spend most of their time indoors [Schwab et al. 1992]. Exposure to indoor air pollutants may have a more important effect on childhood asthma than exposure to outdoor air pollutants [IOM 2000; Etzel 2003]. The primary indoor air pollutants associated with asthma exacerbation include [AAPCEH 2003; Jones 2000]

• Biologic allergens (dust mites, cockroaches, animal dander, mold, etc.),
• Environmental tobacco smoke (ETS),
• Irritant chemicals and fumes, and
• Products from combustion devices.

Biologic allergens can be found throughout the

• Home,
• School, and
• Work and recreational environments

although concentrations of

• Dust mites,
• Cockroaches, and
• Animal dander allergens (pets, mice, rats) vary with geographic location.

However,

• Dust mite allergen,
• Mold, and
• Cat and dog allergens

can be found in most homes, including homes where there are no pets at present [Togias 2003; Weinberger 2003; Nelson 2000].

Sensitization to house dust mites is an important risk factor for asthma exacerbations and the development of asthma. The dust mite grows optimally at warm temperatures and with humidity greater than 50% in cloth-covered objects such as

• Soft toys,
• Upholstered furniture,
• Bedding,
• Mattresses, and
• Carpets [Sporik et al. 1990; Platts-Mills et al. 1995; Duffy et al. 1998].

Cockroach allergens also may increase a child’s risk of developing asthma [IOM 2000, Etzel 2003].

• Cockroach droppings may be one of the most under appreciated allergens in the indoor environment.
• There have been reports of 36% cockroach sensitization rates in inner-city asthmatic children.
• Children with asthma and cockroach allergy exposed to cockroach allergens have more
  • Wheezing,
  • Missed school days,
  • Emergency room visits, and
  • Hospitalizations

than nonsensitized or nonexposed children [IOM 2000; Rosenstreich et al. 1997].

Asthma exacerbation among many children with asthma is causally related to cats [IOM 2000].

• The severity of allergic reactions to cats is greater than reactions to other common domestic pets.
• More than 6 million U.S. residents have allergies to cats, and up to 40% of atopic patients demonstrate skin test sensitivity [Wood and Eggleston 1993].
• However, recent studies have shown that the presence of a cat in the house may decrease the risk of developing asthma [Platts-Mills et al. 2001; Nafstad et al. 2001].

Dogs, rodents, birds, and other furry or feathered animals may contribute in varying degrees to the animal allergens within the home.

• Dogs may have breed-specific allergens, and are less uniformly allergenic than cats [Lindren et al. 1988].
• Rodent allergens can come from pets or pests in the home.
• Birds and feathers have been suggested as allergenic; however the true culprits may be dust mites associated with feathers (including feathers in pillows and clothes)[IOM 2000].

Exposure to molds may lead to allergic sensitization and may exacerbate asthma or allergic rhinitis [IOM 2004].

• At least 60 species of molds have spores thought to be allergenic [Burge 1989].
• Species of particular concern are
  • Penicillium,
  • Aspergillus,
  • Cladosporium, and
  • Alternaria.

Effects of exposure to these species include:

• Nasal congestion,
• Runny nose,
• Conjunctivitis
• Sneezing,
• Lacrimation,
• Wheezing,
• Chest tightness, and
• Shortness of breath.

Among patients studied, children are the most sensitive to mold allergens [Etzel 2003].

Exposure to pollens may cause asthma exacerbations. For pollen to be clinically significant, it must be present in significant numbers and be allergenic. Particles <7µm tend to deposit in the airways [Brooks and Bush 2009]. Ragweed pollen is the most common cause of pollen asthma in the United States. Grass and tree pollens are also a concern in many areas worldwide [Shah and Grammer 2012].

Exposure to environmental tobacco smoke (ETS) is a risk factor for asthma attacks in children [AAPCEH 1997]. Children with asthma and with parents who smoke have more frequent asthma attacks and more severe symptoms [Weitzman et al. 1990; Martinez et al. 1992; Murray and Morrison 1993]. There is clear evidence of an association between exposure to environmental tobacco smoke and the development and exacerbations of asthma. Exposure to ETS also places children at increased risk for

• Sinusitis,
• Otitis media, and
• Bronchiolitis [IOM 2000; Tager et al. 1993].

Improperly used or malfunctioning heating devices are a major source of combustion pollutants indoors. Possible sources of contaminants include

• Gas ranges, especially if used for home heating;
• Improperly vented fireplaces;
• Inefficient or malfunctioning furnaces;
• Stoves burning wood, coal, or other biomass; and
• Unvented or improperly vented kerosene or gas space heaters.

The combustion products from these devices include

• Carbon monoxide (CO),
• Nitrogen dioxide (NO₂),
• Particulate matter, and
• Sulfur dioxide (SO₂).

Although CO is a major health concern, it is not an irritating gas and is not likely by itself to exacerbate asthma. In combination, these combustion products will often exacerbate asthma symptoms [AAPCEH 2003].

Some building materials and home furnishings off-gas formaldehyde [US EPA 1994]. Formaldehyde may exacerbate asthma in some infants and children [Krzyzanowski et al. 1990]. At sufficient concentrations in the air, cleaning products such as chlorine and ammonia may also trigger reactions.

Latex may cause an allergic response either by direct contact or by inhalation of latex particles [Fish 2002]. Symptoms range from skin eruption to bronchospasm and anaphylaxis. Allergic responses around the home may be triggered by

• Gloves,
• Balloons,
• Condoms, and
• Various types of sporting equipment [Landwehr and Boguniewicz 1996].

For the last several decades, high levels of outdoor air pollution have been associated with short-term increases in asthma morbidity and mortality [AAPCEH 1993; Ostro et al. 2001; Tolbert et al. 2000]. Specific exposures to outdoor plant allergens such as organic dusts from

• Castor beans,
• Soybeans, and
• Grains

dramatically illustrate this relationship [Etzel 2003]. Asthma has been shown to be caused and triggered by ambient hazardous air pollutants, as well as industrial releases of

• Aldehydes,
• Metals,
• Uncombusted hydrocarbons,
• Isocyanates, and
• Others [Leikauf et al. 1995].

In some communities, hazardous air pollution is associated with noxious odors, and odors can exacerbate symptoms among some people with asthma [Shusterman 1992].

Air pollution has been implicated as one of the factors responsible for the increase in asthma incidence in most industrialized countries [Salvi 2001]. Clinicians should be aware of the common (criteria) air pollutants that may affect asthmatic patients. The National Ambient Air Quality Standards (NAAQS) are set for six criteria pollutants:

• Ozone (O₃),
• SO₂,
• NO₂,
• CO,
• Particulate matter <10 microns (PM₁₀) and particulate matter <2.5 microns (PM_2.5).

The standards are designed to protect the health of all susceptible groups, including persons with asthma. The Air Quality Index (AQI, Table 2) provides standardized means of communicating health information associated with daily ambient levels of ground-level O₃, SO₂, NO₂, CO, PM₁₀, and PM_2.5 (See Appendix 1). For any reported index value greater than 100, the U.S. Environmental Protection Agency (EPA) determines the index number daily and reports the highest of the:

• Index figures,
• Critical pollutant, and
• Specific groups sensitive to the pollutant [US EPA 1999].

Ozone Some children with asthma (and some children without asthma) have decreases in lung function after exposure to ozone. In the United States, a large fraction of ambient O₃ is the product of photochemical reactions between

• Various nitrogen oxides (NO_x),
• Volatile organic chemicals (VOCs), and
• Ultraviolet light.

Most of the health effects research on O₃ has focused on the short-term effects, such as reductions in FEV₁ and forced vital capacity (FVC). Levels of O₃ are usually greatest on hot summer days and tend to peak in the late afternoon [Etzel 2003; Spektor et al. 1991].

Because of its high solubility, SO₂ mainly irritates the upper airway. The nasal mucosa effectively removes most inspired SO₂ during breathing at rest. Deep penetration to the lung mucosa may occur during moderate exercise. SO₂ has a dose-response association with bronchoconstriction. The amount of SO₂-induced bronchoconstriction is dependent on the level of pre-existing hyper-responsiveness and exercise of the individual. A person without asthma can tolerate a higher concentration of SO₂ before developing symptoms. The bronchoconstrictor response develops within minutes of exposure and resolves within an hour after exposure ends [Ware et al. 1986; Koenig et al. 1990]. The Donora, PA smog disaster in 1948 and the Great London Smog in 1952 are examples of environmental disasters related to air pollution, which claimed many lives.

In contrast to the other pollutants, NO₂ is both an indoor and outdoor air pollutant. Indoor sources of NO₂ include

• Malfunctioning gas stoves,
• Furnaces,
• Fireplaces, and
• Kerosene space heaters.

Most NO₂ health effects are believed to be due to long-term, low-level outdoor exposure. Like the other air pollutants, NO₂ increases bronchial responsiveness during exercise. NO₂ decreases lung function in persons with asthma exposed to concentrations above 0.3 ppm, although there is not a clear dose-response relationship. Short-term exposure to high concentrations of NO₂ induces terminal bronchiolar changes and diffuses alveolar injury. Such high concentrations are generally seen only in accidental exposure, as might occur within confined spaces or in an occupational setting [Etzel 2003; Shima and Adachi 2000].

Particulate matter is a mixture of solid particles and liquid droplets. Particulate matter <10 microns (PM₁₀) is referred to as “course particulate matter” which may result in lower airway exposure [AAPCEH 2003]. PM₁₀ is the standard measure of particulate air pollution used worldwide. Studies suggest that asthma symptoms can be worsened by increases in the levels of PM₁₀, which is a complex mixture of particle types. PM₁₀ has many components and there is no general agreement regarding which component(s) could exacerbate asthma. However, the inflammatory effects of

• Transition metals,
• Hydrocarbons,
• Ultrafine particles, and
• Endotoxin

all present to varying degrees in PM₁₀ – could be important [Donaldson et al. 2000].

Particulate matter <2.5 microns (PM_2.5) is referred to as “fine-particle matter.” Sources of PM_2.5 include

• Industrial and residential combustion,
• Vehicle exhaust,
• Forest and vegetation fires, and
• Atmospheric reactions between gases (SO₂ and NO_x) and VOCs.

PM_2.5 penetrates deeper into the lung than does PM₁₀, potentially causing greater adverse health effects [AAPCEH 2003; Schwartz and Neas 2000]. Several recently published community epidemiologic studies associated adverse effects when PM_2.5 formed a significant portion of the particulate exposure, even though PM₁₀, air concentrations were below NAAQS. Medication use, hospital admissions, and the number of emergency room visits (seen primarily with elderly patients and individuals with cardiopulmonary disease) increased under those conditions [Ware et al. 1986; Dockery et al. 1989].

Exposure to motor traffic emissions can have a significant effect on respiratory function in children and adults.

• Studies show that children living near heavily traveled roadways have significantly higher rates of wheezing and diagnosed asthma [Ciccone et al. 1998].
• Epidemiologic studies suggest that diesel exhaust may be particularly aggravating to children [Brunekreef et al. 1997].
• A child riding in a school bus may be exposed to as much as 4 times the level of diesel exhaust as one riding in a car [NRDC 2001].

Occupational asthma (OA) is defined as a variable airflow limitation and/or airway hyperresponsiveness due to causes and conditions attributable to a particular occupational environment and not to stimuli encountered outside the workplace [Friedman-Jimenez et al. 2000, Mapp et al. 2005].

OA is the most frequently reported respiratory occupational disease in industrialized countries [Bang et al. 2005; NIOSH 2003].

• The annual incidence of OA ranges from 12 to 170 cases per million workers; the estimated mean is 47 cases per million.
• The prevalence of OA is reported at 5% to 15% across many different industries.

The two main types of Occupational Asthma are

1. Immunologic: A latency period that varies from months to years is necessary to acquire immunologically mediated sensitization.
   • IgE mediated: Induced by high molecular weight proteins, and some low molecular weight proteins. Chemicals can form allergens by reacting with cells/proteins and produce IgE. It is associated with other signs and symptoms such as rhinitis and urticaria.
   • Non-IgE: Induced by low molecular weight agents
2. Non-immunologic: There is no latency period.
   • The disease occurs after exposure to high concentrations of work place irritant.
   • Known as irritant induced asthma it can occur after single or multiple irritant exposures. There is a clear temporal association between inhalation exposure and the rapid onset of asthmatic symptoms.
   • The diagnosis is never made in individuals with preexisting asthma.
   • The most common form is “reactive airway dysfunction syndrome (RADS)” which occurs after exposure to high levels of an irritating vapor, fume, or smoke.
   • The symptoms arise within 24 hrs after high-level exposure to irritant and accompanied by eye/nasal irritant symptoms and increased airway responsiveness [Mapp et al. 2005].

Work-exacerbated asthma (WEA) is defined as preexisting or concurrent asthma that is exacerbated by workplace exposure. WEA is common with a median prevalence of 21.5% among adults with asthma [Henneberger et al. 2011].

There are well over 300 agents reported to cause OA [Malo and Chan-Yeung 2006], and an equal or greater number of agents and conditions at work can aggravate existing asthma. Diisocyanates are the leading identified cause of OA worldwide [Johnson et al. 2004; Wisnewski et al. 2006].

Some occupational sensitizers and irritants are

• Aldehydes,
• Animal and vegetable proteins,
• Cleaning agents,
• Detergent enzymes,
• Diisocyanates,
• Epoxy glues,
• Flour,
• Hair dressing products
• Latex,
• Platinum salts, and
• Wood dust.

In 2004, the Institute of Medicine concluded that sufficient evidence exists for associating the presence of mold or other agents in damp buildings to

• Nasal and throat symptoms,
• Cough,
• Wheeze, and
• Asthma symptoms in sensitized people with asthma [IOM 2004].

There has been further work indicating that exposure to damp indoor environments containing mold can lead to the development of asthma since this review was published [Cox-Ganser et al. 2005; Jaakkola 2005].

• A wide range of indoor and outdoor allergens, irritants, as well as cold temperatures, can exacerbate asthma.
• Household exposures to dust mites and cockroach allergens, and the irritant effects of environmental tobacco smoke, contribute significantly to asthma morbidity.
• Occupational asthma is the most common occupational disease in industrialized countries.
• Allergens or irritants in the work environment may cause occupational asthma or exacerbate asthma in those individuals with this preexisting condition.